Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering factor

The aim was to study the effects of radiofrequency (Rf) in a mice strain characterized by age-determined carcinogenesis of lymphatic tissues. Mice were treated with a 1?h/week Rf exposure for 4 months. A group submitted to sham exposure was used as control animals. The evolution of carcinogenesis was followed up to 18 months. The maximal life span of control mice was about 24 months. All dead animals were clinically and histologically examined to give an age-determined comparative quantification of the evolving carcinogenesis. A radiocalcium tracer method permitted the evaluation of Rf effects on transmembrane transport of extracellular calcium at 1 and 24 h after exposure. The determination of induced lipid peroxidation completed this second study. The findings show that Rf provoked an earlier general lymphocyte cell infiltration, formation of lymphoblastic ascites and extranodal tumours of different histological types, as well as an increased early mortality. The results suggest that in Rf-exposed mice, carcinogenesis may be induced earlier and with different pathological forms than in control animals. The modifications in cellular calcium homeostasis and the age-determined thymus involution appear to be important factors involved in this carcinogenesis process.     

Nifedipine diminishes exercise-induced muscle damage in mouse.

The purpose of this study was to evaluate the effects of a calcium channel blocker (nifedipine) on the severity of muscle damage induced by intensive exercise. Male Charles River mice were assigned to four groups (8 mice/group): normal control (C), nifedipine (N), nifedipine and exercise (N + E) and exercise (E). The animals of the C group were not submitted to any exercise nor to drug administration. The animals of the N group received 1 mg.kg-1 per day of nifedipine (Adalat 10 mg, Bayer AG), per os, during 3 days. The mice of the N + E group were submitted to a treadmill run (0 degree slope) at 1000 m.h-1 (80% of their maximal speed) for 1 hour. In this group, the administration of the drug was under the same conditions as for the N group. The administration started 24 h before the run. The E group was submitted to the same exercise protocol as the animals of N + E group. The soleus muscle was excised for light and electron microscopic evaluation using routine histological techniques. In the C and N groups no morphological alterations were detected. In the E group the number of alterations of striated pattern was twice that in the N + E group. The number of fibres with central nuclei was 35% in the E group but only 8% in the N + E group. The total number of damaged fibres was significantly higher in the E group. The results suggest that nifedipine may give protection to exercise-induced skeletal muscle damage in mouse, probably because the blocking of channels impaired Ca2+ influx; and the results of this study therefore confirm earlier contentions about the possible role of calcium ions in producing muscle damage after work.     

Mitochondrial DNA deletions in tissues of mice after ionizing radiation exposure

Purpose: The objective of the study was to estimate the presence of large mtDNA deletions in brain and spleen tissues of mice four months after exposure to 2 and 5?Gy.

Materials and methods: The male BALB/c mice underwent X-ray total-body acute radiation. Four months after irradiation, the mice were decapitated, and the samples of spleen and brain tissues were examined. A long-distance PCR was used to detect mtDNA deletions and their levels in samples of brain and spleen tissues.

Results: Four months after irradiation the levels of mtDNA deletions in the brain and spleen tissues were higher in animals exposed to 5?Gy than in animals at an irradiation dose of 2?Gy and in control mice. The levels of deletions in the mice brain tissues were higher 4 months than 1 month after X-ray exposure to both doses (2 and 5?Gy). In spleen tissues, a higher level of deletions was observed only at an irradiation dose of 5?Gy.

Conclusions: Our data have shown that ionizing radiation induces an increase of mtDNA copies with deletions in tissues of mice four months after the post-irradiation period. The level of deletions depends on the animal age, type of tissue, irradiation dose and length of the post-irradiation period.     

Brain DNA damage and 70-kDa heat shock protein expression in CD1 mice exposed to extremely low frequency magnetic fields

Purpose:?The question of whether exposure to extremely low frequency magnetic fields (ELF-MF), may contribute to cerebral cancer and neurodegeneration is of current interest. In this study we investigated whether exposure to ELF-MF (50 Hz-1 mT) harms cerebral DNA and induces expression of 70-kDa heat shock protein (hsp70).

Materials and methods:?CD1 mice were exposed to a MF (50 Hz-1 mT) for 1 or 7 days (15 h/day) and sacrificed either at the end of exposure or after 24?h. Unexposed and sham-exposed mice were used as controls. Mouse brains were dissected into cerebral cortex-striatum, hippocampus and cerebellum to evaluate primary DNA damage and hsp70 gene expression. Food intake, weight gain, and motor activity were also evaluated.

Results:?An increase in primary DNA damage was detected in all cerebral areas of the exposed mice sacrificed at the end of exposure, as compared to controls. DNA damage, as can be evaluated by the comet assay, appeared to be repaired in mice sacrificed 24?h after a 7-day exposure. Neither a short (15?h) nor long (7 days) MF-exposure induced hsp70 expression, metabolic and behavioural changes.

Conclusions:?These results indicate that in?vivo ELF-MF induce reversible brain DNA damage while they do not elicit the stress response.     

Effects of acute electromagnetic field exposure and movement restraint on antioxidant system in liver,heart, kidney and plasma of Wistar rats: A preliminary report

Purpose:?The aim of the present study was to evaluate the early effects of acute (2?h) exposure to extremely low frequency electromagnetic fields (ELF-EMF), as well as movement restraint (MR) and the combination of both on the antioxidant systems in the plasma, liver, kidney, and heart of rats.

Materials and methods:?Twenty-four adult male Wistar rats were divided in two groups, restrained and unrestrained. The restrained animals were confined into an acrylic tube for 120?min. Half of the animals of each group were exposed to ELF-EMF (60?Hz, 2.4?mT) during the period of restriction. Immediately after treatment, reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS) were measured in tissues.

Results:?GSH concentration was significantly lower in the heart of all experimental animals when compared to the control group; furthermore, the decrease was higher in the liver of restrained animals. SOD activity was lower in the plasma of restrained and EMF exposed animals compared to unrestrained rats. There were no significant differences in CAT activity and TBARS levels among all the experimental groups vs. the control group.

Conclusion:?Two hours of 60?Hz EMF exposure might immediately alter the metabolism of free radicals, decreasing SOD activity in plasma and GSH content in heart and kidney, but does not induce immediate lipid peroxidation. Oxidative stress induced by movement restraint was stronger than that produced by EMF.     

Embryonic implantation, dietary intake, and plasma GH concentration in pregnant mice exposed to hypoxia

Inseminated mice were: 1) exposed to 8% O2, 2) pair fed to mice exposed to 8% O2, 3) fasted at 21% O2 or 4) maintained at 21% O2 (control) between Days 1-3 of pregnancy. The frequency of embryonic implantation sites in mice was reduced by greater than 60% in 8% O2 exposed and pair fed animals, and by 100% in fasted mice. During the initial 24 h of exposure to 8% O2, a significant component of the body weight lost by hypoxic mice was associated with the reduction in dietary intake. The contragestational effects of hypoxia and fasting were attributed to the endocrine consequences of inanition induced by hypophagia and adypsia. Plasma samples collected at 6-h intervals revealed a significant reduction in GH concentration in treatment groups compared to the controls.     

Pulsed high-intensity focused ultrasound enhances uptake of radiolabeled monoclonal antibody to human epidermoid tumor in nude mice.

The aim of this study was to determine if pulsed high-intensity focused ultrasound (HIFU) exposures could enhance tumor uptake of (111)In-MX-B3, a murine IgG1kappa monoclonal antibody directed against the Le(y) antigen. METHODS: MX-B3 was labeled with (111)In, purified, and confirmed for its binding to the antigen-positive A431 cell line. Groups of nude mice were inoculated subcutaneously with A431 tumor cells on both hind flanks. A tumor on one flank was treated with pulsed-HIFU; the other tumor was used as an untreated control. Within 10 min after the HIFU exposure, the mice received intravenous (111)In-MX-B3 for imaging and biodistribution studies. Mice were euthanized at 1, 24, 48, and 120 h after injection for biodistribution studies. RESULTS: The HIFU exposure shortened the peak tumor uptake time (24 vs. 48 h for the control) and increased the peak tumor uptake value (38 vs. 25 %ID/g [percentage injected dose per gram] for the control). The HIFU effect on enhancing tumor uptake was greater at earlier times up to 24 h, but the effect was gradually diminished thereafter. The HIFU effect on enhancing tumor uptake was substantiated by nuclear imaging studies. HIFU also increased the uptake of the antibody in surrounding tissues, but the net increase was marginal compared with the increase in tumor uptake. CONCLUSION: This study demonstrates that pulsed-HIFU significantly enhances the delivery of (111)In-MX-B3 in human epidermoid tumors xenografted in nude mice. The results of this pilot study warrant further evaluation of other treatment regimens, such as repeated HIFU exposures for greater delivery enhancement of antibodies labeled with cytotoxic radioisotopes or pulsed-HIFU exposure in addition to a combined therapy of (90)Y-B3 and taxol to enhance the synergistic effect.     

Chronic exposure of Sprague-Dawley rats to 20 kHz triangular magnetic fields

Purpose:?As a continuing study of 20?kHz triangular magnetic fields (MF) [Lee et al. ], we investigated the chronic toxicity and possible health effects of exposure to 20?kHz MF at the flux density of 30?μT, which is the limit standard for the occupational population in South Korea, with the use of Sprague-Dawley rats.

Materials and methods:?Rats were exposed to 20?kHz triangular MF at 30?μT Root Mean Square for 8?h/day for 18 months. Body and organ weights were measured and urinalysis, hematological and blood biochemistry analyses were performed in individual animals. Histopathological evaluation was also performed for the brain, thymus, lung, heart, liver, kidney, intestine and reproductive organs, including tumour tissue.

Results:?The mortality patterns in male or female rats exposed to magnetic fields were compared to the mortality patterns found in sex-matched sham control animals. Significant alteration of body weight was not observed with MF exposure. No significant differences were seen in sham-exposed and MF-exposed animals based on urological factors, hematological factors and blood biochemistry. Total tumour incidence was not different between sham-exposed and MF-exposed animals.

Conclusion:?Our results suggest that chronic exposure to 20?kHz triangular MF with 30?μT flux density did not increase toxicity in rats.     

Acute mild hypothermia caused by a low dose of X-irradiation induces a protective effect against mid-lethal doses of X-rays, and a low level concentration of ozone may act as a radiomimetic

Acute changes in core body temperature following exposure to a low dose of X-rays were assessed in unanaesthetized and unrestrained mice. Radiotelemetry techniques were used to monitor core body temperature continuously. Following exposure to a 20 cGy dose of X-rays, the mice displayed a rapid and significant reduction in core body temperature relative to the sham-treated (non-irradiated) control animals. The present studies, and those by others, showed that pre-exposure to X-rays at doses as low as 20 cGy may result in a reduced mortality rate following subsequent exposure to X-rays at mid-lethal dose levels. This indicates an increased tolerance to radiation. An additional experiment was conducted to examine whether the reduction in the mortality rate following exposure to mid-lethal doses of radiation could be found when mice were subjected to a stressor, ozone inhalation, which induced a suppression in body temperature. The results showed that following inhalation of ozone at a concentration of 0.5 ppm, 93% of the treated animals survived a mid-lethal dose of radiation, whereas 50% of the sham-control animals died within 30 days. These results suggest that low-dose-induced tolerance to radiation may be dependent on a brief exposure to ozone, and a reduction in core temperature may be necessary to obtain tolerance effects in response to a mid-lethal dose of radiation.     

Persistence of genetic damage in mice exposed to low dose of X rays

Purpose:?The aim of this work was to evaluate the persistence of genetic damage in CBA/J mice treated with a single irradiation of 0.1 or 1 Gy of X rays.

Materials and methods:?Peripheral blood was collected from irradiated and control mice after 30 min, 24 h, 7 days, 1, 3 and 6 months from exposure and analysed by comet assay. To investigate if the whole-body irradiation affect DNA repair, half of the sampled blood cells were in vitro-irradiated with additional 4 Gy and immediately analysed. Six months from exposure haematopoietic organs were sampled for measuring apoptotic index.

Results:?In mice exposed to 1 Gy genetic damage was initially high and decreased during the experimental-time, while in the 0.1 Gy group damage, at first low, persisted and slightly increased. The 0.1 Gy-irradiated mice showed also a time-dependent increasing sensitivity to the in vitro-irradiation. Six months after whole-body irradiation, the percentage of apoptotic cells observed in haematopoietic compartments from 0.1 Gy-irradiated mice was significantly higher compared to controls and to 1 Gy mice.

Conclusions:?Results demonstrated that a single exposure to low-dose might induce long-term damage. Persistence of genetic damage might have relevant implications for estimating risk for low doses.     

Comparative study of radioprotective effects of selenium nanoparticles and sodium selenite in irradiation-induced nephropathy of mice model

Purpose: The current study was undertaken to evaluate radioprotective effects of selenium (Se) nanoparticles in irradiation-induced nephropathy of mice model compared to sodium selenite.

Materials and methods: Forty-five mice were divided into three major groups including control, Se nanoparticle, and sodium selenite. Each major group was further subdivided into three more groups receiving various doses of 0, 2, and 8?Gy gamma irradiation. Both of the supplements were administered intraperitoneally with the dose of 0.1?mg/kg for 14 consecutive days. At the end of each week, the animals were exposed to gamma radiation and 48?h after the last exposure, the animals were humanely euthanized, then blood and renal tissue samples were taken. Serum creatinine, urea, cystatin C, and beta-2-microglobulin levels as well as activities of renal antioxidant enzymes, superoxide dismutase, glutathione peroxidase and catalase, also malondialdehyde level, total antioxidant capacity, renal tissue Se content, and histopathological features were assessed.

Results: The results showed that both of the supplements could normalize aforementioned indices. However, selenium nanoparticles (Se-NPs) were more effective than sodium selenite.

Conclusions: Conclusively, Se-NPs as an emerging potent antioxidant agent can protect against irradiation-induced nephropathy.     

Tracing radiation induced genomic instability in vivo in the haemopoietic cells from fetus to adult mouse

The present experiment was aimed at studying the delayed expression of fetal irradiation induced genomic instability in the mouse haemopoietic cells in vivo. The abdominal area of 14 day pregnant Swiss albino mice was exposed to 0-1.5 Gy of gamma radiation. Chromosomal aberrations were studied in three passages of spleen colonies (short-term repopulating stem cells, STRSC) derived from 24 h post-irradiation fetal liver cells and in the 1-20 months postpartum bone marrow (long-term repopulating stem cells, LTRSC). Irradiation produced a significant and dose-dependent increase in the aberrant metaphases in the first passage spleen colony (CFU-S1) cells, which decreased in subsequent passages and reached normal levels by the third passage (CFU-S3). Bone marrow at 1-6 months postpartum showed similar chromosomal picture in the 0 Gy control and after 0.5-1.5 Gy, but there was a clear increase in aberrant cells from 9 months postpartum in the irradiated groups. Some mice in all irradiated groups showed a 2.5- to 5-fold increase in peripheral leukocyte counts. Bone marrow of these animals exhibited severe aneuploidy, the chromosome number ranging from less than 1n to 6n at 20 months of age. Our results indicate that unstable chromosome aberrations induced in the fetal haemopoietic STRSC are eliminated during subsequent cell divisions. However, genomic instability induced in the LTRSC persists and is expressed as chromosomal aberrations at advanced ages. Induction of chromosome aneuploidy could be an early step in the chain of events leading to adult leukaemia after prenatal irradiation.     

Growth of injected melanoma cells is suppressed by whole body exposure to specific spatial-temporal configurations of weak intensity magnetic fields

Purpose:?To measure the effect of exposure to a specific spatial-temporal, hysiologically-patterned electromagnetic field presented using different geometric configurations on the growth of experimental tumours in mice.

Methods:?C57b male mice were inoculated subcutaneously with B16-BL6 melanoma cells in two blocks of experiments separated by six months (to control for the effects of geomagnetic field). The mice were exposed to the same time-varying electromagnetic field nightly for 3?h in one of six spatial configurations or two control conditions and tumour growth assessed.

Results:?Mice exposed to the field that was rotated through the three spatial dimensions and through all three planes every 2 sec did not grow tumours after 38 days. However, the mice in the sham-field and reference controls showed massive tumours after 38 days. Tumour growth was also affected by the intensity of the field, with mice exposed to a weak intensity field (1–5 nT) forming smaller tumours than mice exposed to sham or stronger, high intensity (2–5?μT) fields. Immunochemistry of tumours from those mice exposed to the different intensity fields suggested that alterations in leukocyte infiltration or vascularisation could contribute to the differences in tumour growth.

Conclusions:?Exposure to specific spatial-temporal regulated electromagnetic field configurations had potent effects on the growth of experimental tumours in mice.     

高压氧对快速减压致中枢神经损伤诱发神经元凋亡的效用

目的研究成年大鼠快速减压致中枢神经系统（CNS）损伤后神经组织细胞凋亡的变化及高压氧（HBO）暴露的效用。方法SD大鼠40只，按随机数字法分为10组，每组4只，即正常对照组、安全减压组、快速减压4个组（1．0MPa暴露5．5min后快速（50S）减至常压后6，24，48，72h组）、HBO4个组（快速减压后5h给予0．25MPa HBO暴露60min）。大鼠均分别于快速减压后6，24，48和72h同期取大脑，用原位末端TUNEL法标记凋亡细胞，光学显微镜下观察形态学改变和高倍镜计数阳性细胞计算凋亡指数。结果正常对照组和安全减压组未标记出TUNEL阳性细胞；快速减压致伤动物6h组CNS组织内仅见少量散在阳性细胞；24h组凋亡指数较6h组增加（P〈0．01）；48和72h组明显增加，达到高峰（P〈0．01）；TUNEL阳性凋亡细胞主要为神经元细胞。HBO暴露组24h组神经元凋亡指数明显较快速减压组相同时间组降低（P〈0．05），48h和72h组降低更加显著（P〈0．01）。结论神经元凋亡是快速减压致CNS损伤中神经元丧失的重要形式之一：HBO暴露能够减少损伤后期的神经元凋亡，对保存神经元、改善预后起到重要作用。     

Low dose gamma-irradiation differentially modulates antioxidant defense in liver and lungs of Balb/c mice

PURPOSE: To evaluate the effect of low-dose (<50 cGy) whole body ?-irradiation on the antioxidant defense system in the liver and the lungs of mice at various post-irradiation intervals. MATERIALS AND METHODS: Male Balb/c mice, 5 - 6 weeks of age, were divided into irradiated and non-irradiated groups. Whole body irradiation was done with gamma-rays from a (60)Co source at doses of 10, 25 and 50 cGy (48.78 cGy/min). Lipid peroxidation and antioxidant status were measured in the liver and the lungs at 4, 12 and 24 h after irradiation. RESULTS: Lipid peroxidation increased by 1.38 and 2.0 fold in lung and liver respectively at 12 h after exposure to 25 cGy. Whole body exposure to 25 and 50 cGy significantly (p < 0.05) increased the hepatic reduced glutathione at 4 h. Reduced glutathione continued to rise until 12 h and returned to the basal level at 24 h, whereas in the lungs it remained elevated until 24 h at 10 and 25 cGy. Antioxidant enzymes activities for superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase increased by 1.22, 1.13, 1.22 and 1.11 fold respectively (p < 0.05) in the liver at 4 h after exposure to 50 cGy and remained elevated at almost the same level up to 12 h after exposure. Surprisingly these antioxidant defense enzymes remained unaltered in the lung at the above radiation doses. CONCLUSIONS: Low-dose whole body gamma-irradiation differentially modulates the antioxidant defense system in the liver and lungs of mice. The induction of endogenous glutathione, immediately after exposure to low-dose -irradiation, may be beneficial in protecting the cells from reactive oxygen species (ROS) induced oxidative stress.     

Persistence of genetic damage in mice exposed to low dose of X rays

PURPOSE: The aim of this work was to evaluate the persistence of genetic damage in CBA/J mice treated with a single irradiation of 0.1 or 1 Gy of X rays. MATERIALS AND METHODS: Peripheral blood was collected from irradiated and control mice after 30 min, 24 h, 7 days, 1, 3 and 6 months from exposure and analysed by comet assay. To investigate if the whole-body irradiation affect DNA repair, half of the sampled blood cells were in vitro-irradiated with additional 4 Gy and immediately analysed. Six months from exposure haematopoietic organs were sampled for measuring apoptotic index. RESULTS: In mice exposed to 1 Gy genetic damage was initially high and decreased during the experimental-time, while in the 0.1 Gy group damage, at first low, persisted and slightly increased. The 0.1 Gy-irradiated mice showed also a time-dependent increasing sensitivity to the in vitro-irradiation. Six months after whole-body irradiation, the percentage of apoptotic cells observed in haematopoietic compartments from 0.1 Gy-irradiated mice was significantly higher compared to controls and to 1 Gy mice. CONCLUSIONS: Results demonstrated that a single exposure to low-dose might induce long-term damage. Persistence of genetic damage might have relevant implications for estimating risk for low doses.     

Effects of mechanical vibration on rat plasma calcium, magnesium, phosphate, and xanthine oxidase.

Sprague-Dawley rats were vibrated for 4 min in one of 12 combinations of G levels (+/-2, +/-4, or +/-8 GX) and frequency ranges (12-61, 62-111, 112-161, or 162-211 HZ). The animals were restrained and conscious during vibration. Plasma calcium, magnesium and inorganic phosphate concentrations as well as xanthine oxidase activities were determined for each animal at various times before and after vibration. Vibration at specific G levels induced physiological changes in plasma calcium, magnesium, and xanthine oxidase levels. Plasma inorganic phosphate concentrations appeared to increase with an increase in the displacement of vibration. All of the effects observed occurred within 24 h of vibration treatment. An effect of the frequency of vibration was not observed with any of the parameters examined. Factors involved in performing the experiments also were able to induce certain physiological changes, viz., the level of plasma calcium and xanthine oxidase activity.     

Effects of 50Hz magnetic fields on cancer induced by ionizing radiation in mice

Purpose : To evaluate the effects of 50Hz magnetic fields (MF) on the development of cancer induced by ionizing radiation. Materials and methods : A total of 150 female CBA/S mice were randomized into three equal groups at the age of 3–5 weeks. One of the groups served as a 'cage-control group'. The two other groups were exposed to ionizing radiation in the beginning of the study. One of these two groups was exposed 24 h per day, for 1.5 years, to a 50 Hz vertical MF, the intensity of which varied regularly between 1.3, 13 and 130 μ T. The other served as a control group and was sham-exposed to MF in similar, but unenergized, exposure racks. Body weights, clinical signs, and food and water consumption were recorded regularly. Haematological examination, and the histopathological analysis of all lesions and major tissues were performed on all animals. Results : MF exposure did not increase the incidence of any primary neoplasms. However, the incidence of basophilic liver foci, a probable pre-neoplastic change in liver, was increased. The incidence of hepatocellular adenomas was unchanged, whereas the incidence of hepatocellular carcinomas was slightly, but not statistically significantly, elevated. Conclusions : It is concluded that overall the results of this study do not support a role for MF as a tumour promoter.     

Prolonged Retention of 77Br labelled bromphenol blue in tumor tissue

The present investigations were undertaken to determine if there is an accumulation or retention of ⁷⁷Br labelled bromphenol blue in neoplastic tissue, in order to examine its usefulness as a tumor imaging agent. After labelling the dye was intravenously injected into control animals and into mice with experimentally induced pulmonary tumors which served as a model for these studies.Some hours after the injection, when most of the substance had been eliminated from normal tissue, there was a distinct retention of the dye in the tumors of the lung. The ratios of the activity concentrations in the lungs of animals with tumors vs those in the lungs of control animals increased to 1.95 within a time of 24 h after injection of the dye. The activity concentration in the tumor tissue was 5 times that in the lung tissue. This elevated uptake could be seen in some scintigrams of lungs.     

Multiple blood-proteins approach for early-response exposure assessment using an in vivo murine radiation model

Purpose:?The aim was to evaluate the utility of multiple blood-protein biomarkers for early-response assessment of radiation exposure using a murine radiation model system.

Material and methods:?BALB/c male mice (8–10 weeks old) were exposed to whole-body ⁶⁰Co γ-rays (10 cGy min^?1) over a broad dose range (0–7 Gy). Blood protein biomarkers (i.e., Growth Arrest and DNA Damage Inducible Gene 45 or GADD45α, interleukin 6 or IL-6, and serum amyloid A or SAA) were measured by enzyme linked immunosorbent assay (ELISA) at 4, 24, 48, and 72 h after total-body irradiation (TBI).

Results:?Time- and dose-dependent increases in the protein targets were observed. The use of multiple protein targets was evaluated using multiple linear regression analysis to provide dose-response calibration curves for dose assessment. Multivariate discriminant analysis demonstrated enhanced dose-dependent separation of irradiated animals from control as the number of biomarkers increased.

Conclutions:?Results from this study represent a proof-of-concept for multiple blood-proteins biodosimetry approach. It was demonstrated for the first time that protein expression profile could be developed not only to assess radiation exposure in male BALB/c mice but also to distinguish the level of radiation exposure, ranging from 1–7 Gy.